Miyajima T, Tsujino T, Saito K, Yokoyama M
First Department of Internal Medicine, Kobe University School of Medicine, Japan.
Hypertens Res. 2001 Sep;24(5):537-42. doi: 10.1291/hypres.24.537.
This study was designed to clarify the effects of orally administered eicosapentaenoic acid (EPA) on blood pressure, intracellular sodium content, and cell membrane fatty acid composition in patients with essential hypertension. After a 4-week run-in period, a study group of 17 male patients was assigned to an 8-week treatment with EPA (2.7 g/day) or placebo in a randomized, double-blind fashion with a crossover at week 4. Systolic blood pressure (SBP) was lower after treatment with EPA than after treatment with placebo (152.9+/-17.3 vs. 162.6+/-20.6 mmHg; p<0.01), while diastolic blood pressure was not statistically different. Compared with the placebo treatment, EPA supplementation resulted in a decrease in intraerythrocyte sodium content (R-Na; 11.17+/-0.63 vs. 10.44+/-1.28 nmol/l cells; p<0.05) accompanied by an increase (p<0.001) in erythrocyte membrane EPA content. The increase in membrane EPA content was related to the decrease in SBP (r=-0.52, p<0.05) and the decrease in R-Na (r=-0.57, p<0.02) during EPA treatment. The decrease in R-Na correlated positively with the decrease in SBP (r=0.54, p<0.05), and correlated negatively with the change in Na+-K+ ATPase activity (r= -0.59, p<0.02). However, the change in Na+-K+ ATPase activity did not directly correlate with the change in membrane EPA content. In conclusion, oral EPA supplementation increased membrane EPA content and reduced SBP in patients with essential hypertension. Based on the association between the increase in membrane EPA content and the decrease in intracellular sodium concentration, EPA may lower blood pressure by altering the activities of the membrane sodium transport systems.
本研究旨在阐明口服二十碳五烯酸(EPA)对原发性高血压患者血压、细胞内钠含量及细胞膜脂肪酸组成的影响。经过4周的导入期后,17名男性患者的研究组被随机、双盲地分配接受EPA(2.7克/天)或安慰剂治疗8周,并在第4周进行交叉。治疗后,EPA治疗组的收缩压(SBP)低于安慰剂治疗组(152.9±17.3对162.6±20.6 mmHg;p<0.01),而舒张压无统计学差异。与安慰剂治疗相比,补充EPA导致红细胞内钠含量降低(R-Na;11.17±0.63对10.44±1.28 nmol/升细胞;p<0.05),同时红细胞膜EPA含量增加(p<0.001)。在EPA治疗期间,膜EPA含量的增加与SBP的降低(r=-0.52,p<0.05)和R-Na的降低(r=-0.57,p<0.02)相关。R-Na的降低与SBP的降低呈正相关(r=0.54,p<0.05),与Na+-K+ATP酶活性的变化呈负相关(r=-0.59,p<0.02)。然而,Na+-K+ATP酶活性的变化与膜EPA含量的变化无直接相关性。总之,口服补充EPA可增加原发性高血压患者的膜EPA含量并降低SBP。基于膜EPA含量增加与细胞内钠浓度降低之间的关联,EPA可能通过改变膜钠转运系统的活性来降低血压。